Abstract: This disclosure relates to managing brain injury. In certain embodiments, this disclosure relates to methods comprising administering an effective amount of an inhibitor of sphingosine-1-phoshate signaling, an inhibitor of retinoic-acid-receptor-related orphan receptors ? or ?, and/or an inhibitor of tPA microglial activation to a subject in need thereof. Typically, the subject is a neonate or a neonate born prematurely.

Abstract: The c-Jun NH2-terminal kinase (JNK) group of MAP kinases are activated by exposure of cells to environmental stress. The role of JNK in the brain was examined by targeted disruption of the gene that encodes the neuronal isoform JNK3. It was found that JNK3 is required for the normal response to seizure activity. Methods of screening for molecules and compounds that decrease JNK3 expression or activity are described. Such molecules or compounds are useful for treating disorders involving excitotoxicity such as seizure disorders, Alzheimer's disease, Huntington disease, Parkinson's disease, and ischaemia.

Abstract: Plasminogen activators as potential therapeutic targets in neonatal hypoxia ischemia (HI) brain injury. Use of plasminogen activator inhibitor-1 (PAI-1) to ameliorate HI encephalopathy related disease. Use of PAI-1 as preventive treatment of cerebral palsy (CP).

Abstract: The c-Jun NH2-terminal kinase (JNK) group of MAP kinases are activated by exposure of cells to environmental stress. The role of JNK in the brain was examined by targeted disruption of the gene that encodes the neuronal isoform JNK3. It was found that JNK3 is required for the normal response to seizure activity. Methods of screening for molecules and compounds that decrease JNK3 expression or activity are described. Such molecules or compounds are useful for treating disorders involving excitotoxicity such as seizure disorders, Alzheimer's disease, Huntington disease, Parkinson's disease, and ischaemia.

Abstract: The c-Jun NH2-terminal kinase (JNK) group of MAP kinases are activated by exposure of cells to environmental stress. The role of JNK in the brain was examined by targeted disruption of the gene that encodes the neuronal isoform JNK3. It was found that JNK3 is required for the normal response to seizure activity. Methods of screening for molecules and compounds that decrease JNK3 expression or activity are described. Such molecules or compounds are useful for treating disorders involving excitotoxicity such as seizure disorders, Alzheimer's disease, Huntington disease, Parkinson's disease, and ischaemia.